Simmondsin

Last updated
Simmondsin
Simmondsin.svg
Clinical data
ATC code
  • none
Identifiers
  • (2Z)-2-[(2S,3R,4S,6R)-2-hydroxy-3,4-dimethoxy-6-[(2R,3R,4S,5S,6R)-3,4,
CAS Number
PubChem CID
ChemSpider
UNII
Chemical and physical data
Formula C16H25NO9
Molar mass 375.374 g·mol−1
3D model (JSmol)
  • N#C\C=C2/[C@H](O[C@@H]1O[C@@H]([C@@H](O)[C@H](O)[C@H]1O)CO)C[C@H](OC)[C@H](OC)[C@H]2O
  • InChI=1S/C16H25NO9/c1-23-9-5-8(7(3-4-17)11(19)15(9)24-2)25-16-14(22)13(21)12(20)10(6-18)26-16/h3,8-16,18-22H,5-6H2,1-2H3/b7-3+/t8-,9+,10-,11+,12-,13+,14-,15+,16-/m1/s1
  • Key:KURSRHBVYUACKS-XGYNEUJOSA-N
   (verify)

Simmondsin is a component of jojoba seeds (pronounced "ho-HO-bah") ( Simmondsia chinensis ). While it had been considered toxic due to jojoba seed meal causing weight loss in animals, in recent years its appetite suppressant effect has also been researched as a potential treatment for obesity. [1] It is thought to reduce appetite by increasing levels of cholecystokinin. [2] [3] [4] [5]

Related Research Articles

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Cholecystokinin is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein. Cholecystokinin, formerly called pancreozymin, is synthesized and secreted by enteroendocrine cells in the duodenum, the first segment of the small intestine. Its presence causes the release of digestive enzymes and bile from the pancreas and gallbladder, respectively, and also acts as a hunger suppressant.

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Proglumide (Milid) is a drug that inhibits gastrointestinal motility and reduces gastric secretions. It acts as a cholecystokinin antagonist, which blocks both the CCKA and CCKB subtypes. It was used mainly in the treatment of stomach ulcers, although it has now been largely replaced by newer drugs for this application.

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CI-988 (PD-134,308) is a drug which acts as a cholecystokinin antagonist, selective for the CCKB subtype. In animal studies it showed anxiolytic effects and potentiated the analgesic action of both morphine and endogenous opioid peptides, as well as preventing the development of tolerance to opioids and reducing symptoms of withdrawal. Consequently, it was hoped that it might have clinical applications for the treatment of pain and anxiety in humans, but trial results were disappointing with only minimal therapeutic effects observed even at high doses. The reason for the failure of CI-988 and other CCKB antagonists in humans despite their apparent promise in pre-clinical animal studies is unclear, although poor pharmacokinetic properties of the currently available drugs are a possible explanation, and CCKB antagonists are still being researched for possible uses as adjuvants to boost the activity of other drugs.

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References

  1. "Simmondsin From Jojoba - Checked for Appetite Suppression". United States Department of Agriculture, Agricultural Research Service.
  2. Cokelaere MM, Busselen P, Flo G, Daenens P, Decuypere E, Kühn E, Van Boven M (December 1995). "Devazepide reverses the anorexic effect of simmondsin in the rat". The Journal of Endocrinology. 147 (3): 473–7. doi:10.1677/joe.0.1470473. PMID   8543917.
  3. Flo G, Vermaut S, Van Boven M, Daenens P, Buyse J, Decuypere E, et al. (August 1998). "Comparison of the effects of simmondsin and cholecystokinin on metabolism, brown adipose tissue and the pancreas in food-restricted rats". Hormone and Metabolic Research. 30 (8): 504–8. doi:10.1055/s-2007-978921. PMID   9761380. S2CID   260166054.
  4. Flo G, Van Boven M, Vermaut S, Daenens P, Decuypere E, Cokelaere M (April 2000). "The vagus nerve is involved in the anorexigenic effect of simmondsin in the rat". Appetite. 34 (2): 147–51. doi:10.1006/appe.1999.0299. PMID   10744903. S2CID   42949049.
  5. Boozer CN, Herron AJ (July 2006). "Simmondsin for weight loss in rats". International Journal of Obesity. 30 (7): 1143–8. doi:10.1038/sj.ijo.0803251. PMID   16462820. S2CID   1282460.